**4. Tendon healing and latest molecular updates**

Tendon healing undergoes overlapping inflammation, proliferation and remodelling [12] via two mechanisms -extrinsic and intrinsic [7]. Within the first week of injury, blood vessels within the tendon and tendon sheath form a thrombus at the injury site which acts to recruit vasodilators and proinflammatory cells [12]. These cells migrate to the injury site and help with removal of necrotic tissue, fibrin, clot and cellular debris through phagocytosis. Canine models have shown that angiogenic factors, such as vascular endothelial growth factor (VEGF), help initiate the vascular invasion to the site of injury [13].

In the third week, the tendon enters the proliferative stage whereby the fibroblasts rapidly proliferate, synthesis immature collagen in an unorganised manner, and assist with the production of extracellular matrix (ECM) [14]. This initial laid down collagen is type III collagen which is a weaker form of the type I collagen present in native tendons. The combination of type III collagen and previously initiated vascular network leads to scar formation within the tendon- this initially decreases its strength before the tendon enters the final stage of healing

At weeks six to eight, the remodelling stage predominates. Here type I collagen fibres are reorganised in a longitudinal manner along the long axis of the tendon with collagen fibrils crosslinking to one another to increase the strength of the tendon [14]. It is during this stage that adhesions between the tendon and its sheath become more apparent

#### **4.1. Intrinsic healing**

**2.6. Flexor zones**

24 Essentials of Hand Surgery

in the resting posture.

both FDS and FDP.

**3.1. Patterns of injury**

**3.2. Lacerations**

**3.3. Avulsion injuries**

added Type V [11] (**Table 1**).

(TCL).

includes the C3 and A5 Pulleys and the FDP tendon.

**Zone 4** is the area deep to the TCL i.e. the carpal tunnel.

**3. Types of flexor tendon injury**

tendons and major neuromuscular structures

The volar surface of the hand is divided into five anatomic zones from distal to proximal. When describing a zone for an injury it is referred to by the zone that it would lie in the hand

**Zone 1** commences at the fingertip and ends at the insertion of FDS on the middle phalanx. It

**Zone 2** is from the insertion of the FDS to the proximal aspect of the A1 pulley. It contains

**Zone 3** is from the proximal A1 pulley to the distal limit of the transverse carpal ligament

A sharp laceration to a flexor tendon is the most common cause of injury (for example from a knife or glass). It is rare for blunt injuries to divide the tendon but the significant crushing to the tendon can result in adhesions if not managed properly. Avulsion injuries are also common.

Lacerations may be complete or partial [2]. Lacerations within Zone 1 only involve FDP and those in Zone 2 usually involve both FDP and FDS tendons as well as any neuromuscular injury. Tears within the fibro-osseous sheath are more prone to restrictive adhesions than those within Zones 3–5. However, small lacerations in Zones 3–5 frequently involve multiple

Four factors determine the prognosis of avulsion injuries of flexor tendons: the extent of retraction of the proximal tendon, the remaining blood supply, the time interval between

The FDP tendon is prone to avulsing from its insertion into the distal phalanx and is commonly called a "jersey injury" [9]. This occurs when the distal phalanx is extended at the DIP joint while the FDP is maximally contracted. This avulsion may involve a fragment of bone. Jersey finger most commonly affects the ring finger because it is the most proximal digit when the hand is flexed. Leddy and Packer have classified jersey injuries into Types I to III [9]. This classification has been modified by Smith who added a Type IV injury [10] and Al-Qattan who

trauma and surgery, and the presence and size of any osseous fragments [2].

**Zone 5** is from the proximal edge of the TCL to the musculotendinous junction.

Intrinsic healing involves only the tenocytes (fibroblasts) within the tendon itself and depends on the migration and proliferation of cells from the epitenon and endotenon [7, 14]. Epitenon tenocytes produce collagen earlier than those of the endotenon. Tenocytes of the endotenon produce large and more mature collagen than epitenon cells. In any event, both endotenon and epitenon tenocytes establish an extracellular matrix and internal neovascular network. Intrinsic healing results in improved biomechanics within the sheath, including tendon gliding. Movement of the tendon within the sheath improves synovial circulation and therefore the delivery of nutrients.

(AAV) vectors in a chicken model demonstrated that healing strength was improved without increased adhesion formation [24]. Tang and colleagues [25] also used AAV vectors harbouring rat basic fibroblast growth factor (bFGF) to transfect chicken flexor tendons. Their results

Flexor Tendon Injuries

27

http://dx.doi.org/10.5772/intechopen.73392

• **Tissue engineering:** Basile et al. [26] used a devitalised acellular allograft tendon containing recombinant AAV expressing growth and differentiation factor-5 as a delivery model. They were able to repopulate the graft, decrease scar tissue and enhance the gliding property relative to the control graft. Zhao et al. [27] demonstrated that lubricin combined with hyaluronic acid and bone marrow stromal cells stimulated with growth and differentiation factoir-5 can significantly improve gliding function in canine flexor models. However there were substantial decreases in repair strength compared to control In large animal models, synthetic membranes [28] and tissue-engineered synovial membranes [29] have been

An accurate history and examination allows for planning of surgical approach. Though it is preferable for early tendon repair [30], immediate repair of a flexor tendon may be contraindicated in extensively contaminated wounds or those with substantial injury (involving two or more elements of skin, nerve, artery, vein, flexor tendons, extensor mechanism, bone or joint). Delayed presentation may also warrant surgical reconstruction of a flexor tendon due to proximal myostatic muscle-tendon retraction resulting inability to bring the proximal and distal

It is important to perform a clinical examination of the traumatised hand before the administration of local anaesthesia to accurately identify and document neurologic or vascular injury [3]. Firstly, any volar laceration of the hand or wrist requires careful observation of the flexor cascade. In the normal cascade, each finger is slightly more flexed than the adjacent radial

To assess FDS, the FDP must be blocked from acting on the PIP joint. This is done by isolating the affected finger by holding all other fingers in extension and asking the patient to flex the PIP joint. By repeating the test against resistance, applied to the middle phalanx, partial lacerations of the tendon can be identified as it will elicit increased pain. FDP, responsible for flexion of the DIP, is tested in a similar manner to FDS. The middle phalanx is held in extension and the patient instructed to flex the DIP joint of each finger. Again, this can be done against resistance to identify partial tendon lacerations. FPL is tested by stabilising the proximal phalanx of the thumb and instructing the patient to flex the IP joint. However, a more reliable test of FPL function is using the 'O' sign where the patient is asked to make an O shape between their thumb and index finger. This O shape is only possible if the FPL is intact. This test is more reliable than asking the patient to flex the IP joint as there are trick movements that can cause a flicker of movement at the IP joint,

showed a moderate reduction in adhesions.

shown to decrease peritendinous adhesions.

finger when the wrist is neutral or slightly extended.

**5. History and examination**

causing diagnostic confusion.

stumps together.

#### **4.2. Extrinsic healing**

Extrinsic healing involves the invasion of fibroblasts and inflammatory cells into the site of injury from the surrounding synovium, paratenon and tendon sheath [7, 14]. This produces scarring and peritendinous adhesions which may impair tendon movement, gliding and nutrition. It is thought that extrinsic healing predominates in the earlier stages of tendon healing. Extrinsic healing also predominates when tendons are immobilised after injury or repair. The extrinsic mechanism is activated earlier and is responsible for initial adhesions, the highly cellular collagen matrix and the high-water content of the injury site [7, 14]. The intrinsic mechanism then causes tenocytes from within the tendon to invade the defect and produce collagen which reorganises and aligns longitudinally to maintain fibrillar continuity and produce a healed tendon [15].

#### **4.3. Research trends**

Careful surgical technique and initiation of early motion after surgical repair of flexor tendon injuries have been the main strategies for decreasing tendon adhesions after surgical repair. Recent research has concentrated on improving the healing response within the tendon whilst decreasing the adhesion formation between the tendon and its sheath.


(AAV) vectors in a chicken model demonstrated that healing strength was improved without increased adhesion formation [24]. Tang and colleagues [25] also used AAV vectors harbouring rat basic fibroblast growth factor (bFGF) to transfect chicken flexor tendons. Their results showed a moderate reduction in adhesions.

• **Tissue engineering:** Basile et al. [26] used a devitalised acellular allograft tendon containing recombinant AAV expressing growth and differentiation factor-5 as a delivery model. They were able to repopulate the graft, decrease scar tissue and enhance the gliding property relative to the control graft. Zhao et al. [27] demonstrated that lubricin combined with hyaluronic acid and bone marrow stromal cells stimulated with growth and differentiation factoir-5 can significantly improve gliding function in canine flexor models. However there were substantial decreases in repair strength compared to control In large animal models, synthetic membranes [28] and tissue-engineered synovial membranes [29] have been shown to decrease peritendinous adhesions.
